Hu Jianping, Aguirre Maria, Peto Charles, Alonso Jose, Ecker Joseph, Chory Joanne
Plant Biology Laboratory, Howard Hughes Medical Institute, Laboratory of Neuronal Structure and Function, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Science. 2002 Jul 19;297(5580):405-9. doi: 10.1126/science.1073633.
The nuclear protein DET1 is a central repressor of photomorphogenesis in plants. We have identified the molecular lesion in ted3, a mutation that dominantly suppresses the phenotypes of det1-1. TED3 encodes a peroxisomal protein (AtPex2p) essential for Arabidopsis growth. Developmental defects and the abnormal expression of many genes in det1 are rescued by ted3. ted3 also partially suppresses another pleiotropic de-etiolated mutant cop1. Thus, peroxisomes, whose functions are still largely unexplored, play a key role in a photomorphogenetic pathway negatively regulated by the DET1 and COP proteins.
核蛋白DET1是植物光形态建成的核心抑制因子。我们已经鉴定出ted3中的分子损伤，ted3是一个显性抑制det1-1表型的突变体。TED3编码一种对拟南芥生长至关重要的过氧化物酶体蛋白（AtPex2p）。ted3挽救了det1中的发育缺陷和许多基因的异常表达。ted3还部分抑制了另一个多效性去黄化突变体cop1。因此，其功能仍在很大程度上未被探索的过氧化物酶体，在由DET1和COP蛋白负调控的光形态建成途径中起关键作用。
